Insulin-like growth factor I promotes cord blood T cell maturation through monocytes and inhibits their apoptosis in part through interleukin-6

Abstract

Background: The functional immaturity of T cells contributes to the susceptibility of neonates to infections and the less severe graft-versus-host disease associated with cord blood (CB) transplantation. We have previously reported that insulin-like growth factor -I (IGF-I) promotes the phytohaemagglutinin (PHA)-induced CB T cell maturation and inhibits their apoptosis in mononuclear cell (MC) culture. We hypothesized that the effects of IGF-I may be mediated by accessory cells and soluble factors.

The Neurotoxic Effects of Estrogen on Ischemic Stroke in Older Female Rats Is Associated with Age-Dependent Loss of Insulin-Like Growth Factor-1

“…Following ischemia, several cell death and cell protective responses are generated in brain tissue, and the eventual size and severity of the infarct reflects the balance between these opposing cellular processes. For example, inflammation is a critical post-ischemic event, and IGF-1 is reported to promote T-cell maturation and delay apoptotic cell death of neutrophils (Himpe et al, 2008; Law et al, 2008), which is consistent with its growth promoting actions, but may create a less favorable environment for neurons post-ischemia. Thus, early IGF-1 treatment may hinder the development of a full neuroprotective effect.…”

Serum concentrations and tissue expression of components of insulin-like growth factor-axis in females with type 2 diabetes mellitus and obesity: The influence of very-low-calorie diet

“…Previously it has been reported that IGF-1 was involved in inflammation-induced angiogenic processes in the porcine model of sterile heart inflammation (Kluge et al, 1997) and in the development of endothelial cell dysfunction by enhancing pro-inflammatory cytokine signal transduction (Che et al, 2002). Positive effects of IGF-1 have been described on the stimulation of natural killer cell cytotoxicity and proliferation of human peripheral blood mononucelar cells (Koojiman et al, 1992a) as well as on the maturation and inhibition of apoptosis of cord blood monocyte-derived dendritic cells (Law et al, 2008). Moreover, in the presence of IGF-1 monocytes isolated from GH-deficient patients differentiated into macrophages (Serri et al, 2004).…”

Neuroprotective Effects of Intranasal IGF-1 against Neonatal Lipopolysaccharide-Induced Neurobehavioral Deficits and Neuronal Inflammation in the Substantia Nigra and Locus Coeruleus of Juvenile Rats

“…9). IGF-1 has been shown to modulate neonatal immune responses in maturation processes and inflammation by suppressing pro-inflammatory Th1 cytokine IL-6 and stimulating anti-inflammatory Th2 cytokine IL-10 [53, 54]. Increased IGF-1 production through liposomal IGF-1 gene transfer has been shown to regulate pro- and anti-inflammatory cytokine expression in the burn wound and improve healing, suggesting that IGF-1 decreases local inflammation [55].…”